Differential effects of acute and chronic exercise on plasticity-related genes in the rat hippocampus revealed by microarray
Differential effects of acute and chronic exercise on plasticity-related genes in the rat hippocampus revealed by microarray
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DOI：
10.1046/j.1460-9568.2002.02158.x
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发表时间：
2002-09-01
影响因子：
3.4
通讯作者：
Gómez-Pinilla, F
中科院分区：
文献类型：
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作者：
Molteni, R;Ying, Z;Gómez-Pinilla, F
研究确定了急性和慢性自愿运动对海马区基因表达的影响。使用包含1176个主要在大脑中表达的cDNA的微阵列检测了暴露在转轮上3、7和28天的啮齿动物的RNA。用Taqman逆转录聚合酶链式反应或核糖核酸酶保护实验对所选基因的表达进行定量。最大的上调发生在与突触运输相关的基因(突触蛋白I、突触素和突触素)、信号转导途径(钙/钙调蛋白依赖的蛋白激酶II，CaM-KII；丝裂原激活/细胞外信号调节的蛋白激酶，MAP-K/ERK I和II；蛋白激酶C，PKC-Delta)或转录调节基因(环磷酸腺苷反应元件结合蛋白，CREB)。与谷氨酸能系统相关的基因上调(N-甲基-d-天冬氨酸受体NMDAR-2A和NMDAR-2B和兴奋性氨基酸载体1，EAAC1)，而与γ-氨基丁酸(GABA)系统相关的基因下调(GABA(A)受体，谷氨酸脱羧酶GAD65)。脑源性神经营养因子(BDNF)是唯一一个基因在各个时间点持续上调的营养因子。这些结果，再加上大多数上调的基因都与脑源性神经营养因子存在公认的相互作用，表明脑源性神经营养因子在运动对大脑可塑性的影响中发挥了核心作用。基因表达的时间分布似乎描绘了一种机制，通过这种机制，特定的分子通路在运动后被激活。例如，CaM-K信号系统在急性和慢性运动期间似乎是活跃的，而MAP-K/ERK系统在长期运动中似乎更重要。
Studies were performed to determine the effects of acute and chronic voluntary periods of exercise on the expression of hippocampal genes. RNAs from rodents exposed to a running wheel for 3, 7 and 28 days were examined using a microarray with 1176 cDNAs expressed primarily in the brain. The expression of selected genes was quantified by Taqman RT-PCR or RNase protection assay. The largest up-regulation was observed in genes involved with synaptic trafficking (synapsin I, synaptotagmin and syntaxin); signal transduction pathways (Ca2+ /calmodulin-dependent protein kinase II, CaM-KII; mitogen-activated/extracellular signal-regulated protein kinase, MAP-K/ERK I and II; protein kinase C, PKC-delta) or transcription regulators (cyclic AMP response element binding protein, CREB). Genes associated with the glutamatergic system were up-regulated (N -methyl-d-aspartate receptor, NMDAR-2A and NMDAR-2B and excitatory amino acid carrier 1, EAAC1), while genes related to the gamma-aminobutyric acid (GABA) system were down-regulated (GABA(A) receptor, glutamate decarboxylase GAD65). Brain-derived neurotrophic factor (BDNF) was the only trophic factor whose gene was consistently up-regulated at all timepoints. These results, together with the fact that most of the genes up-regulated have a recognized interaction with BDNF, suggest a central role for BDNF on the effects of exercise on brain plasticity. The temporal profile of gene expression seems to delineate a mechanism by which specific molecular pathways are activated after exercise performance. For example, the CaM-K signal system seems to be active during acute and chronic periods of exercise, while the MAP-K/ERK system seems more important during long-term exercise.